Abstract
The scheme for mouse mammary tumorigenesis has been extended to include 3-mefhylcholanthrene (MCA) as an effective tumorigenic agent. Methylcholanthrene is a very poor noduligenic agent in intact virgin BALB/c mice, and the hyperplastic alveolar nodules induced have low tumor-producing capabilities. However, D1 mammary-nodule outgrowths responded to MCA with a relatively high rate of tumor production (50%). Prolonged hormone stimulation by pituitary isografts increased the tumor incidence in MCA-treated D1 nodule outgrowths in a similar fashion, as was shown previously for mammary tumor virus (MTV)-positive and nodule-inducing virus (NIV)-positive D1 nodule outgrowths exposed to prolonged hormone stimulation. When MCA was given to MTV-positive mice bearing D1 nodule outgrowths, the effect appeared to be additive, rather than synergistic. There was no evidence that MCA acted hormonally in the neoplastic transformation. Rather, the results suggested that MCA acted on the D1 nodule cell population to increase the production of tumors from this population, whereas hormone stimulation acted synergistically with MTV and NIV to increase tumor formation from D1 nodule outgrowths.
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